A Rosetta Patient Speaks: The Cerebrovascular Theory of Intracranial Hypertension

A Rosetta Patient Speaks: The Cerebrovascular Theory of Intracranial Hypertension

Cerebrovasular Theory of Intracranial Hypertension, Part 2: Leading to The Danger Zone

It’s really simple. Damage/squeeze (“stenosis”) the main veins that drain the brain and a situation is created where the damaged veins can’t drain blood OUT as fast as the heart pumps it IN. Blood backs up, the brain swells, and pressurized CSF. The only cause? Dunno, but interesting that Diamox, a nasty drug used to “reduce CSF production”, is actually a diuretic used to treat blood pressure. Looking at the huge torrent of blood that flows through the brain, comparing it to what amounts to a quiet pool of CSF that changes at a snails pace, CSF MADE from blood to begin with, and it begs the question: why the focus on reducing precious CSF if the cause is actually damaged veins that can’t drain blood away adequately during periods of increased blood flow to the brain? Here’s the long story:

During my “experiential residency” in the study of Intracranial Pressure Dysregulation Disorders, it has become apparent that certain areas of the brain appear to be more susceptible to increased CSF pressure. However, I don’t believe that an imbalance in CSF production and absorption is the principal cause of my particular ICPDD, but rather a symptom, the result of an imbalance in the blood flowing into the brain vs. blood flowing out of the brain. The tenets of my current Cerebrovascular Induced Intracranial Hypertension are a direct extension of Dr. Mark Wilson’s ’s publication “Monro-Kellie 2.0“, and my personal experience as patient with an Intracranial Pressure Dysregulation Disorder that my neurosurgeon tell me does not fit any of the criteria for currently recognized conditions such as IIH. These tenets are as follow; facts are derived from “Brain Facts and Figures” (https://faculty.washington.edu/chudler/facts.html):

Two Fluid Postulate: The cranium contains two fluids, blood and cerebrospinal fluid, in approximately equal volumes, ~ 150 cc 1, in patients without ICPDD and “intact” ICP Autoregulation.

Static Nature of CSF: Cerebrospinal Fluid volume is assumed to be essentially constant for this discussion This does not dismiss the possibility that a net positive or negative CSF dynamic is not a contributory factor in ICPDD. However, CSF turnover only averages .35 cc/minute1, leading to the next tenet…

Blood vs. CSF: Cerebrovascular blood flow dynamics greatly outweigh CSF dynamics. Blood flow into the brain is 15-20% of cardiac output, 750-1000 cc/minute1, meaning that CSF dynamics represent a mere .05% of the change in volume of fluid In the brain per minute. This is a known fact apparently forgotten or ignored according to Dr. Wilson.

Cerebrovascular Network: Our brains demand a lion’s share of oxygen and nutrients, provided by blood flow. These nutrients are distributed through a network of blood vessels. In order to provide each cell of the brain with oxygen/nutrients, blood vessels must be in extremely close proximity to each cell. The vascular network is extremely complex, and is estimated to comprise 100,000 miles of blood vessels, the majority of them only wide enough to allow blood cells to pass through single file, about 6um (micrometers): 6/1000s of a millimeter. Main arteries and veins into/out of the brain can be as large as an inch, then branch out continually into ever smaller vessels to provide nutrients to each of the approximately 100 billion neurons in our brains. All of this is accomplished with a mere 150 cc of blood fluid volume, which flows through this cerebrovascular network at 750-1000 cc per minute.

Volumetric Balance: to maintain equilibrium of the volume of blood in the brain, the total venous outflow capacity has to equal the total arterial inflow ***This is the critical tenet of this theory: blood flowing into the brain MUST flow out at an equal rate****

Venous Outflow Insufficiency: The 800 lb Gorilla in your head: Understanding the previous tenets, the critical nature of sufficient venous outflow becomes apparent. Arteries and veins are vastly different in nature and function. Arteries are thick walled, contain smooth muscle, and dilate/contract in response to our nervous system and biochemicals (hormones). Veins are thin walled tubes of cells; their diameter is susceptible to posture, gravity, and the actual rate of flow through them (as per Bernoulli’s Principle). Veins are susceptible to damage by trauma, posture, and anatomical factors including Body Mass Index. When Venous Outflow is insufficient to match Arterial Inflow, there is a net increase in the VOLUME of blood in the brain.

Intracranial Contents, The Volumetric Paradox, and The Physical Nature of The Brain: The adult skull is approximately 1700 cc in volume; the brain occupies 1400 cc; blood, 150 cc; csf, 150 cc. However, there is a paradox: the 1400 cc of brain volume also contains a majority of the 150 cc of bloodwithin the skull. The brain itself is mostly water, 77-78%, contained within the network of neurons that comprise the tangible portion of the brain. These neurons are chiefly lipids (10-12%), proteins (8%), and 4-5% a combination of carbohydrates, “soluble organic substances”, and inorganic salts. The consistency of the brain is about the same as firm tofu (http://www.human-memory.net/brain.html); slightly elastic, with a degree of resilience. The brain “floats” in cerebrospinal fluid that not only surrounds it, but again, a paradox: approximately 2% of the brain’s volume is hollow “ventricles” (https://www.ncbi.nlm.nih.gov/pubmed/21120804), spaces where CSF is produced and distributed through the brain and then to the space around the brain and spinal cord (subarachnoid space). Thus, the 1400 cc volume of the brain also contains about 28 cc of cerebrospinal fluid. This is the basis for the Volumetric Paradox: 15% human brain’s volume is comprised of blood and cerebrospinal fluid.

The End Game: When Venous Outflow Insufficiency meets the Volumetric Paradox: Tofu and Internal Pressure: Our brains are soft, mildly resilient structures. They require enormous amounts of oxygen and nutrients, delivered by arterial blood flow. Blood depleted of nutrients and oxygen is then drained by veins. Cerebrospinal fluid, a crucial but poorly understood component of this system, changes at a snail’s pace compared to blood flow, and thus for this discussion will be considered a static innocent bystander for what happens next: Venous Outflow Insufficiency. If, for some reason, the main veins that drain the brain (sorry, it’s been a looooonnnnnnngggggg week, I’m a little punchy, I just couldn’t help it) are unable to handle the arterial blood flowing into the brain, a serious cascade of pernicious events follow. Blood begins to back up in the brain’s cerebrovascular network. Pressure within the network increases. This pressure cause the blood vessels in the brain to become engorged and expand, similar to the way that the veins in your arm start to bulge when a tourniquet is applied in order to draw blood for testing. The next part is my speculation, but under equal pressures, it seems that thin walled, passive veins enlarge more than thick walled arteries that contain active muscle. All within the 100,000 mile network of the Cerebrovascular network. As the vessels expand, pressure is exerted outward on the tofu-textured brain. The brain matter itself is forced to expand into the only spaces available to it: the outer subarachnoid space and the inner ventricles. The cerebrospinal fluid, the innocent bystander, is now “bitch-slapped” around by this building pressure, referred to as EOMAP, or “End Organ Mean Arterial Pressure”. Newton’s 3rd Law of Physics states that every action is met with an equal and opposite reaction; in the case of Venous Outflow Insufficiency, this means that as cerebrospinal fluid becomes pressurized by brain tissue expanding due to a backup of blood in the vessels of the brain, the CSF “pushes back”, trapping brain structure between the”Devil” of the engorged and expanding blood vessels and “The Deep Blue Sea” of the now-pressurized CSF both outside AND inside of our brains. And….

Voila’: Intracranial Hypertension. By definition. Caused not by CSF, the equivalent of a small pool of still water, but rather by the sudden blockage of the torrential river of blood that flows through our brains. There is much, much more to the dynamics of this process and how the negative process feeds upon itself, but this concept is already a recognized process in an extremely acute ICPDD, Acute Mountain Disease and its associated deadly consequence of HACE, High Altitude Cerebral Edema. For the time being, understanding this process as a potential cause of ICPDDs including IIH, NPH, pick-your-alpahabetic-combination-of-Hs, is critical to understanding what happens as its result. This will be explored in the next topic on ShuntWhisperer.com, “The Danger Zones.”

This post, this topic, this site, is dedicated to the memory of my wife, Trina Haddix, who died as a result of complications related to an untreated ICPDD. Her story will be told on TrinasPage.com in the coming weeks. I miss you baby, I love you so much. I will not let you be forgotten.